Abstract | Full Text | Full Text PDF | PubMed | Scopus (24) | Google ScholarSee all References Withdrawal of sexual stimulation causes a return of sympathetic tone and degradation of cGMP, predominantly by phosphodiesterase type 5 (PDE-5) within the trabecular smooth muscle.11x11Nehra, A. Intracavernosal therapy: when oral agents fail. Curr Urol Rep. 2001; 2: 468–472
Relation between erectile dysfunction prevalence and type of coronary syndrome (A). Time interval (months) between erectile dysfunction and coronary artery disease symptom onset in chronic coronary syndrome according to the number of vessels involved (B). ACS, acute coronary syndrome; CCS, chronic coronary syndrome, G1: ACS and 1-VD; G2: ACS and 2-,3-VD; G3: CCS. VD, vessel disease; C: the control group with normal coronary angiography. With permission from Montorsi et al.15
DHEA. Testosterone is essential for a healthy libido and normal sexual function, and erectile dysfunction sufferers known to have low testosterone improve when placed on prescription testosterone replacement therapy. Similarly, studies have shown that taking over-the-counter supplements containing DHEA, a hormone that the body converts to testosterone and estrogen, can help alleviate some cases of ED. But DHEA can cause problems, including suppression of pituitary function, acne, hair loss and its long-term safety is unknown, says McCullough. For this reason, many experts discourage use of the supplements.

Following the breakthrough in ED treatment using PDE5-inhibitors, Western medicine has now moved on to a new frontier of regenerative medicine, with stem cell and gene therapy leading the way (25). There is a practical need for novel therapy as a significant portion of diabetic or post-prostatectomy ED patients do not respond to oral pharmacotherapy. To date, stem cells derived from different sites including adipose tissue-derived stem cells, bone marrow mesenchymal stem cells and muscle-derived stem cells have been investigated using animal models for ED, to study their effects on neural, vascular, endothelial or smooth muscle regeneration (25,26).


The views expressed in this article intend to highlight alternative studies and induce conversation. They are the views of the author and do not necessarily represent the views of hims, and are for informational purposes only, even if and to the extent that this article features the advice of physicians and medical practitioners. This article is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment, and should never be relied upon for specific medical advice.

The cardiovascular adverse effects of sildenafil use have been studied extensively. Phosphodiesterase type 5, although located primarily in the genitalia, also can be found throughout the systemic vasculature, although other PDEs predominate there10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Crossref | PubMed | Scopus (1) | Google ScholarSee all References Angiotensin-converting enzyme inhibitors also have low rates of secondary ED associated with their use in both animal and human studies.45x45Srilatha, B, Adaikan, PG, Arulkumaran, S, and Ng, SC. Sexual dysfunction related to antihypertensive agents: results from the animal model. Int J Impot Res. 1999; 11: 107–113
An equally valuable observation though, is the fact that sexual dysfunction could indeed indicate asymptomatic CV disease. A solid amount of evidence accumulated over the last years has pointed out towards that trend moving, hesitatingly though, sexual dysfunction in the surface of scientific interest. As such, commonly under-reported, under-recognized and under-treated, sexual dysfunction could indeed play its role in cardiovascular risk assessment and stratification.
There are two kinds of penis implants. One kind is a rigid but flexible rod implanted in the penis. You bend it up for sex or down for daily living. The other kind is an inflatable implant. The device stores fluid in a reservoir under the skin of your abdomen or scrotum. You press on the reservoir to pump fluid into cylinders in the penis. That creates an erection. A valve drains the fluid out of the penis when you're done.
Yet another common erectile dysfunction treatment that can be used in combination with oral drugs is a vacuum pump. This device consists of a plastic cylinder, a pump, a set of constriction bands, and a water-soluble lubricant. The lubricant is applied to the base of the penis to help form an airtight seal. The cylinder is placed over the flaccid penis and held tight against the pelvis. The pump is used to create a vacuum within the cylinder, drawing blood into the penis. Once the penis is engorged with blood, a constriction band is rolled off the cylinder to near the base of the penis. The constriction band is helpful for men with venous leakage, in which blood flows out of the penis as fast as it flows in. However, it should be left on for no more than 30 minutes at a time.

When it comes to scientific development, in Western medicine, an analytic approach is often used to identify and resolve medical challenges. A hypothesis is first derived through general observations of a phenomenon. A research plan is then carefully designed and data collected. Once sufficient data is collected, critical statistical evaluations are done and conclusions are drawn (4). Every aspects of a disease entity are studied from macroscopic to microscopic views, down to the cellular and molecular levels. The deep understanding of the role of cGMP-specific phosphodiesterase type 5 enzymes in ED and the use of phosphodiesterase-5 inhibitors in treatment of ED exemplifies the success of this approach.


Getting blood glucose under control is a good anti-ED tactic. Men with diabetes and poor blood glucose control are two to five times as likely to have ED as those with good control. One study in a group of men who had had type 1 diabetes for up to 15 years with minor complications found that intensive blood glucose control lowered the risk of ED compared with conventional treatment. A study in men with type 2 diabetes found that lowering A1C (average blood glucose in the past two to three months) below 7 percent and reducing blood pressure through a combination of medication, diet, and exercise improved sexual functioning.
There are currently two models of the inflatable penile prosthesis (IPP), namely, the two-piece IPP vs. the three-piece IPP. The three-piece IPP consists of a pair of corporal cylinders, a scrotal pump and an abdominal reservoir filled with saline. Owing to the presence of the reservoir, the corporal cylinders can be completely deflated to give the patient the physiological flaccid state when not in use, and likewise a maximally turgid state when inflated (21). The two-piece IPP lacks an abdominal reservoir and is often offered in patients with whom placement of reservoir is challenging or not possible such as following radical cysto-prostatectomy with orthotopic ileal neobladder creation, or patients who had previous open book fracture of the pelvis with metal implants. The concept of ectopic reservoir placement has allowed many of these men the option for three-piece IPP placement (22). Technological advances have improved mechanical reliability, reduced prosthesis infection risk and offered excellent patient and partner satisfaction rate (23).
Physical and emotional stress — whether over-exercising, under-sleeping or just dealing with everyday stressors like work and a busy schedule — causes an increase in “stress hormones,” including cortisol and adrenaline. Stress can lower desire for sex. This is because stress can contribute to fatigue or preoccupation with other tasks. It can also significantly affect blood flow by increasing inflammation.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (46) | Google ScholarSee all References The Princeton Consensus Panel provided guidelines (Table 4) for physicians regarding patients who are being evaluated for their level of risk in resuming sexual activity.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F
In the early years of my cardiology practice, I was surprised by the number of men with heart disease who also suffered from impotence. In fact, being incapable of having an erection was the norm rather than the exception after heart attack. In those days, impotence was widely attributed to the psychological depression that often followed heart attack.
Unfortunately, government agencies often are slow to respond to new scientific information and economic and political forces make it difficult for our population to receive clear information informing them that heart disease is nutritionally induced and totally avoidable with dietary excellence. Sadly, even the American Heart Association advocates a diet that has been shown to actually increase heart disease.
Several other facts support the close relationship between sexual dysfunction and CV disease. Endothelial dysfunction mediated by decreased nitric-oxide bioavailability as well as atherosclerotic lesions constitute a common pathophysiologic substrate affecting both CV disease and erectile dysfunction, a disease considered to be primarily of vascular origin[76,80-82]. Several traditional CV risk factors (diabetes mellitus, hypertension, dyslipidemia, and smoking) are frequently found in individuals with erectile dysfunction, conferring a detrimental cardiovascular burden to them. More interestingly, the increased cardiovascular risk observed in those patients is independent of the aforementioned CV risk factors[81-88].
The wide range of prevalence rates noted among the studies can be attributed to a number of factors. First, prevalence rates are affected by the sensitivity and specificity of methods used to assess ED.1 In addition, a number of these studies used medical record review to identify patients with ED, as opposed to anonymous patient reports. It has been shown in other disease states that patients tend to underreport ED when questioned directly by their providers.3 Therefore, the use of validated questionnaires that are either self-administered in an anonymous, neutral setting or administered by an objective third-party interviewer are preferred.
Testosterone therapy in hypogonadism modulates metabolic components associated with CV risk. The majority of prospective clinical studies indicates that treatment achieving testosterone levels within physiological limits has beneficial or neutral effects on a lipid profile other than HDL-C, beneficial or neutral effects on inflammatory mediators, and generally beneficial effects on glycaemic state.25 The lean body mass is typically increased in hypogonadal subjects, and visceral adiposity is decreased in several studies and unchanged in the remainder. Such metabolic effects have raised interest on the potential impact on cardiovascular health. Regarding symptoms in patients with pre-existing cardiovascular conditions (angina or heart failure) TTh has been either neutral or beneficial.25 Regarding CVD risk, available clinical trial data indicate that the use of testosterone in middle-aged to elderly men does not increase cardiovascular risk25 with the exception of one study in very frail (substantial limitation of mobility and a high rate of comorbidities) elderly subjects that used an off-label high, and rapid escalation, dosing regimen.46 Prospective data from large, well-designed, long-term trials of TTh are warranted.
In some cases, however, these drugs may be unsuitable for patients with heart disease. If you are considering one of these drugs and you have heart disease, as many diabetics do, be sure to tell your doctor. In rare cases, the pills may create “priapism,” a prolonged and painful erection lasting six hours or more (although reversible with prompt medical attention).
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